tbuckley/cabot-search huggingface dataset:
AXL and Error-Prone DNA Replication Confer Drug Resistance and Offer Strategies to Treat EGFR-Mutant Lung Cancer
Authors: Ashish Noronha, Nishanth Belugali Nataraj, Joo Sang Lee, Benny Zhitomirsky, Yaara Oren, Sara Oster, Moshit Lindzen, Saptaparna Mukherjee, Rainer Will, Soma Ghosh, Arturo Simoni-Nieves, Aakanksha Verma, Rishita Chatterjee, Simone Borgoni, Welles Robinson, Sanju Sinha, Alexander Brandis, D. Lucas Kerr, Wei Wu, Arunachalam Sekar, Suvendu Giri, Youngmin Chung, Diana Drago-Garcia, Brian P. Danysh, Mattia Lauriola, Michelangelo Fiorentino, Andrea Ardizzoni, Moshe Oren, Collin M. Blakely, Jideofor Ezike, Stefan Wiemann, Laxmi Parida, Trever G. Bivona, Rami I. Aqeilan, Joan S. Brugge, Aviv Regev, Gad Getz, Eytan Ruppin, Yosef Yarden
Journal: Cancer Discovery (2022)

Anticancer therapies have been limited by the emergence of mutations and other adaptations. In bacteria, antibiotics activate the SOS response, which mobilizes error-prone factors that allow for continuous replication at the cost of mutagenesis. We investigated whether the treatment of lung cancer with EGFR inhibitors (EGFRi) similarly engages hypermutators. In cycling drug-tolerant persister (DTP) cells and in EGFRi-treated patients presenting residual disease, we observed upregulation of GAS6, whereas ablation of GAS6's receptor, AXL, eradicated resistance. Reciprocally, AXL overexpression enhanced DTP survival and accelerated the emergence of T790M, an EGFR mutation typical to resistant cells. Mechanistically, AXL induces low-fidelity DNA polymerases and activates their organizer, RAD18, by promoting neddylation. Metabolomics uncovered another hypermutator, AXL-driven activation of MYC, and increased purine synthesis that is unbalanced by pyrimidines. Aligning anti-AXL combination treatments with the transition from DTPs to resistant cells cured patient-derived xenografts. Hence, similar to bacteria, tumors tolerate therapy by engaging pharmacologically targetable endogenous mutators. EGFR-mutant lung cancers treated with kinase inhibitors often evolve resistance due to secondary mutations. We report that in similarity to the bacterial SOS response stimulated by antibiotics, endogenous mutators are activated in drug-treated cells, and this heralds tolerance. Blocking the process prevented resistance in xenograft models, which offers new treatment strategies. This article is highlighted in the In This Issue feature, p. 2483.
Evolutionary Genomics of a Subdivided Species
Authors: Takahiro Maruki, Zhiqiang Ye, Michael Lynch
Journal: Molecular Biology and Evolution (2022)

The ways in which genetic variation is distributed within and among populations is a key determinant of the evolutionary features of a species. However, most comprehensive studies of these features have been restricted to studies of subdivision in settings known to have been driven by local adaptation, leaving our understanding of the natural dispersion of allelic variation less than ideal. Here, we present a geographic population-genomic analysis of 10 populations of the freshwater microcrustacean Daphnia pulex, an emerging model system in evolutionary genomics. These populations exhibit a pattern of moderate isolation-by-distance, with an average migration rate of 0.6 individuals per generation, and average effective population sizes of ∼650,000 individuals. Most populations contain numerous private alleles, and genomic scans highlight the presence of islands of excessively high population subdivision for more common alleles. A large fraction of such islands of population divergence likely reflect historical neutral changes, including rare stochastic migration and hybridization events. The data do point to local adaptive divergence, although the precise nature of the relevant variation is diffuse and cannot be associated with particular loci, despite the very large sample sizes involved in this study. In contrast, an analysis of between-species divergence highlights positive selection operating on a large set of genes with functions nearly nonoverlapping with those involved in local adaptation, in particular ribosome structure, mitochondrial bioenergetics, light reception and response, detoxification, and gene regulation. These results set the stage for using D. pulex as a model for understanding the relationship between molecular and cellular evolution in the context of natural environments.
Real-world data on the effectiveness, safety and drug survival of dupilumab: an analysis from the TREATgermany registry
Authors: Dora Stölzl, Nicole Sander, Annice Heratizadeh, Eva Haufe, Inken Harder, Susanne Abraham, Luise Heinrich, Andreas Kleinheinz, Andreas Wollenberg, Elke Weisshaar, Knut Schäkel, Konstantin Ertner, Franca Wiemers, Julia Wildberger, Margitta Worm, Ralph von Kiedrowski, Isaak Effendy, Andrea Asmussen, Matthias Augustin, Mario Pawlak, Michael Sticherling, Alexander Zink, Melanie Hilgers, Christiane Handrick, Sven Quist, Beate Schwarz, Petra Staubach-Renz, Magnus Bell, Sun-Hei Hong-Weldemann, Bernhard Homey, Jens-Joachim Brücher, Jochen Schmitt, Thomas Werfel, Stephan Weidinger
Journal: British Journal of Dermatology (2022)

This interim analysis from the atopic dermatitis registry TREATgermany shows robust long-term efficacy, favourable safety and high persistence of dupilumab under real life conditions.
Butyrate acts through HDAC inhibition to enhance aryl hydrocarbon receptor activation by gut microbiota-derived ligands
Authors: Morgane Modoux, Nathalie Rolhion, Jeremie H. Lefevre, Cyriane Oeuvray, Petr Nádvorník, Peter Illes, Patrick Emond, Yann Parc, Sridhar Mani, Zdenek Dvorak, Harry Sokol
Journal: Gut Microbes (2022)

Aryl hydrocarbon receptor (AhR) is a critical player in the crosstalk between the gut microbiota and its host. However, factors regulating AhR within the gut, which is a complex metabolomic environment, are poorly understood. This study investigates the effect of a combination of metabolites on the activation mechanism of AhR. AhR activity was evaluated using both a luciferase reporter system and mRNA levels of AhR target genes on human cell lines and human colonic explants. AhR activation was studied by radioligand-binding assay, nuclear translocation of AhR by immuofluorescence and protein co-immunoprecipitation of AhR with ARNT. Indirect activation of AhR was evaluated using several tests and inhibitors. The promoter of the target gene CYP1A1 was studied both by chromatin immunoprecipitation and by using an histone deacetylase HDAC inhibitor (iHDAC). Short-chain fatty acids, and butyrate in particular, enhance AhR activity mediated by endogenous tryptophan metabolites without binding to the receptor. This effect was confirmed in human intestinal explants and did not rely on activation of receptors targeted by SCFAs, inhibition of AhR degradation or clearance of its ligands. Butyrate acted directly on AhR target gene promoter to reshape chromatin through iHDAC activity. Our findings revealed that butyrate is not an AhR ligand but acts as iHDAC leading to an increase recruitment of AhR to the target gene promoter in the presence of tryptophan-derived AhR agonists. These data contribute to a novel understanding of the complex regulation of AhR activation by gut microbiota-derived metabolites.
CAR T-cell Therapy Meets Clonal Hematopoiesis
Authors: Ugur Uslu, Carl H. June
Journal: Blood Cancer Discovery (2022)

Summary: Clonal hematopoiesis of indeterminate potential (CHIP) is common in patients with hematologic malignancies. Recent publications provide evidence that CHIP may affect chimeric antigen receptor T-cell therapy efficacy and that the incidence of treatment-related toxicities such as cytokine release syndrome and immune effector-cell associated neurotoxicity syndrome may be affected. See related article by Saini et al., p. 385 (8).
Donor Macrophages Modulate Rejection After Heart Transplantation
Authors: Benjamin J. Kopecky, Hao Dun, Junedh M. Amrute, Chieh-Yu Lin, Andrea L. Bredemeyer, Yuriko Terada, Peter O. Bayguinov, Andrew L. Koenig, Christian C. Frye, James A.J. Fitzpatrick, Daniel Kreisel, Kory J. Lavine
Journal: Circulation (2022)

Cellular rejection after heart transplantation imparts significant morbidity and mortality. Current immunosuppressive strategies are imperfect, target recipient T cells, and have adverse effects. The innate immune response plays an essential role in the recruitment and activation of T cells. Targeting the donor innate immune response would represent the earliest interventional opportunity within the immune response cascade. There is limited knowledge about donor immune cell types and functions in the setting of cardiac transplantation, and no current therapeutics exist for targeting these cell populations.
Nuclear Receptor NR1D1 Regulates Abdominal Aortic Aneurysm Development by Targeting the Mitochondrial Tricarboxylic Acid Cycle Enzyme Aconitase-2
Authors: Ling-Yue Sun, Yu-Yan Lyu, Heng-Yuan Zhang, Zhi Shen, Guan-Qiao Lin, Na Geng, Yu-Li Wang, Lin Huang, Ze-Hao Feng, Xiao Guo, Nan Lin, Song Ding, An-Cai Yuan, Lan Zhang, Kun Qian, Jun Pu
Journal: Circulation (2022)

Background: Metabolic disorder increases the risk of abdominal aortic aneurysm (AAA). NRs (nuclear receptors) have been increasingly recognized as important regulators of cell metabolism. However, the role of NRs in AAA development remains largely unknown. Methods: We analyzed the expression profile of the NR superfamily in AAA tissues and identified NR1D1 (NR subfamily 1 group D member 1) as the most highly upregulated NR in AAA tissues. To examine the role of NR1D1 in AAA formation, we used vascular smooth muscle cell (VSMC)–specific, endothelial cell–specific, and myeloid cell–specific conditional Nr1d1 knockout mice in both AngII (angiotensin II)– and CaPO 4 -induced AAA models. Results: Nr1d1 gene expression exhibited the highest fold change among all 49 NRs in AAA tissues, and NR1D1 protein was upregulated in both human and murine VSMCs from AAA tissues. The knockout of Nr1d1 in VSMCs but not endothelial cells and myeloid cells inhibited AAA formation in both AngII- and CaPO 4 -induced AAA models. Mechanistic studies identified ACO2 (aconitase-2), a key enzyme of the mitochondrial tricarboxylic acid cycle, as a direct target trans-repressed by NR1D1 that mediated the regulatory effects of NR1D1 on mitochondrial metabolism. NR1D1 deficiency restored the ACO2 dysregulation and mitochondrial dysfunction at the early stage of AngII infusion before AAA formation. Supplementation with αKG (α-ketoglutarate, a downstream metabolite of ACO2) was beneficial in preventing and treating AAA in mice in a manner that required NR1D1 in VSMCs. Conclusions: Our data define a previously unrecognized role of nuclear receptor NR1D1 in AAA pathogenesis and an undescribed NR1D1-ACO2 axis involved in regulating mitochondrial metabolism in VSMCs. It is important that our findings suggest αKG supplementation as an effective therapeutic approach for AAA treatment.
Predictive Utility of a Validated Polygenic Risk Score for Long-Term Risk of Coronary Heart Disease in Young and Middle-Aged Adults
Authors: Sadiya S. Khan, Courtney Page, Daniel M. Wojdyla, Yosef Y. Schwartz, Philip Greenland, Michael J. Pencina
Journal: Circulation (2022)

Background: Understanding the predictive utility of previously derived polygenic risk scores (PRSs) for long-term risk of coronary heart disease (CHD) and its additive value beyond traditional risk factors can inform prevention strategies. Methods: Data from adults 20 to 59 years of age who were free of CHD from the FOS (Framingham Offspring Study) and the ARIC (Atherosclerosis Risk in Communities) study were analyzed. Because the PRS was derived from samples of predominantly European ancestry, individuals who self-reported White race were included. The sample was stratified by age and cohort: young (FOS, 20–39 years [median, 30 years] of age), early midlife (FOS, 40–59 years [median, 43] years of age), and late midlife (ARIC, 45–59 years [median, 52 years] of age). Two previously derived and validated prediction tools were applied: (1) a 30-year traditional risk factor score and (2) a genome-wide PRS comprising &gt;6 million genetic variants. Hazard ratios for the association between each risk estimate and incident CHD were calculated. Predicted and observed rates of CHD were compared to assess discrimination for each model individually and together with the optimism-corrected C index (95% CI). Results: Among 9757 participants, both the traditional risk factor score (hazard ratio per 1 SD, 2.60 [95% CI, 2.08–3.27], 2.09 [95% CI, 1.83–2.40], and 2.11 [95% CI, 1.96–2.28]) and the PRS (hazard ratio, 1.98 [95% CI, 1.70–2.30], 1.64 [95% CI, 1.47–1.84], and 1.22 [95% CI, 1.15–1.30]) were significantly associated with incident CHD in young, early midlife, and late midlife, respectively. Discrimination was similar or better for the traditional risk factor score (C index, 0.74 [95% CI, 0.70–0.78], 0.70 [95% CI, 0.67–0.72], and 0.72 [95% CI, 0.70–0.73]) compared with an age- and sex-adjusted PRS (0.73 [95% CI, 0.69–0.78], 0.66 [95% CI, 0.62–0.69], and 0.66 [95% CI, 0.64–0.67]) in young, early-midlife, and late-midlife participants, respectively. The ΔC index when PRS was added to the traditional risk factor score was 0.03 (95% CI, 0.001–0.05), 0.02 (95% CI, −0.002 to 0.037), and 0.002 (95% CI, −0.002 to 0.006) in young, early-midlife, and late-midlife participants, respectively. Conclusions: Despite a statistically significant association between PRS and 30-year risk of CHD, the C statistic improved only marginally with the addition of PRS to the traditional risk factor model among young adults and did not improve among midlife adults. PRS, an immutable factor that cannot be directly intervened on, has minimal clinical utility for long-term CHD prediction when added to a traditional risk factor model.
Single-cell multimodal analysis identifies common regulatory programs in synovial fibroblasts of rheumatoid arthritis patients and modeled TNF-driven arthritis
Authors: Marietta Armaka, Dimitris Konstantopoulos, Christos Tzaferis, Matthieu D. Lavigne, Maria Sakkou, Anastasios Liakos, Petros P. Sfikakis, Meletios A. Dimopoulos, Maria Fousteri, George Kollias
Journal: Genome Medicine (2022)

Synovial fibroblasts (SFs) are specialized cells of the synovium that provide nutrients and lubricants for the proper function of diarthrodial joints. Recent evidence appreciates the contribution of SF heterogeneity in arthritic pathologies. However, the normal SF profiles and the molecular networks that govern the transition from homeostatic to arthritic SF heterogeneity remain poorly defined.
Engineered extracellular vesicles and their mimetics for cancer immunotherapy
Authors: Chunping Liu, Yichao Wang, Longmei Li, Dongyue He, Jiaxin Chi, Qin Li, Yixiao Wu, Yunxuan Zhao, Shihui Zhang, Lei Wang, Zhijin Fan, Yuhui Liao
Journal: Journal of Controlled Release (2022)
Re: Sylvia H.J. Jochems, Josef Fritz, Christel Häggström, Bengt Järvholm, Pär Stattin, Tanja Stocks. Smoking and Risk of Prostate Cancer and Prostate Cancer Death: A Pooled Study. Eur Urol. In press. https://doi.org/10.1016/j.eururo.2022.03.033
Authors: Paulius Bosas, Gintaras Zaleskis, Dainius Characiejus
Journal: European Urology (2022)
Re: Pawel Rajwa, Benjamin Pradere, Giorgio Gandaglia, et al. Intensification of Systemic Therapy in Addition to Definitive Local Treatment in Nonmetastatic Unfavourable Prostate Cancer: A Systematic Review and Meta-analysis. Eur Urol 2022;82:82–96
Authors: Vedang Murthy, Srinivas Chilukuri, Priyamvada Maitre
Journal: European Urology (2022)
Single-cell multiome of the human retina and deep learning nominate causal variants in complex eye diseases
Authors: Sean K. Wang, Surag Nair, Rui Li, Katerina Kraft, Anusri Pampari, Aman Patel, Joyce B. Kang, Christy Luong, Anshul Kundaje, Howard Y. Chang
Journal: Cell Genomics (2022)

Genome-wide association studies (GWASs) of eye disorders have identified hundreds of genetic variants associated with ocular disease. However, the vast majority of these variants are noncoding, making it challenging to interpret their function. Here we present a joint single-cell atlas of gene expression and chromatin accessibility of the adult human retina with more than 50,000 cells, which we used to analyze single-nucleotide polymorphisms (SNPs) implicated by GWASs of age-related macular degeneration, glaucoma, diabetic retinopathy, myopia, and type 2 macular telangiectasia. We integrate this atlas with a HiChIP enhancer connectome, expression quantitative trait loci (eQTL) data, and base-resolution deep learning models to predict noncoding SNPs with causal roles in eye disease, assess SNP impact on transcription factor binding, and define their known and novel target genes. Our efforts nominate pathogenic SNP-target gene interactions for multiple vision disorders and provide a potentially powerful resource for interpreting noncoding variation in the eye.
Association between socioeconomic status and health behaviour change before and after non-communicable disease diagnoses: a multicohort study
Authors: Danyang Wang, Xiaochen Dai, Shiva Raj Mishra, Carmen C W Lim, Rodrigo M Carrillo-Larco, Emmanuela Gakidou, Xiaolin Xu
Journal: The Lancet Public Health (2022)

Behavioural risk factors of non-communicable diseases (NCDs) are socially patterned. However, the direction and the extent to which socioeconomic status (SES) influences behaviour changes before and after the diagnosis of NCDs is not clearly understood. We aimed to investigate the influence of SES on behaviour changes (physical inactivity and smoking) before and after the diagnosis of major NCDs.In this multicohort study, we pooled individual-level data from six prospective cohort studies across 17 countries. We included participants who were diagnosed with either diabetes, cardiovascular disease, chronic lung disease, or cancer after recruitment. Participants were surveyed every 2 years. Education and total household wealth were used to construct SES. We measured behaviour changes as whether or not participants continued or initiated physical inactivity or smoking after NCD diagnosis. We used multivariable logistic regression models to estimate odds ratios (ORs), prevalence ratios (PRs), and 95% CIs for the associations between SES and continuation or initiation of unfavourable behaviours.We included 8107 individuals recruited between March, 2002, and January, 2016. Over the 4-year period before and after NCD diagnosis, 886 (60·4%) of 1466 individuals continued physical inactivity and 1018 (68·8%) of 1480 participants continued smoking; 1047 (15·8%) of 6641 participants with physical activity before diagnosis initiated physical inactivity after diagnosis and 132 (2·0%) of 6627 non-smokers before diagnosis initiated smoking after diagnosis. Compared with participants with high SES, those with low SES were more likely to continue physical inactivity (244 [70·3%] of 347 vs 23 [50.0%] of 46; PR 1·41 [95% CI 1·05-1·99]; OR 2·28 [1·18-4·41]), continue smoking (214 [75·4%] of 284 vs 39 [60·9%] of 64; PR 1·27 [1·03-1·59]; OR 2·08 [1·14-3·80]), but also to initiate physical inactivity (188 [26·1%] of 720 vs 47 [7·4%] of 639; PR 3·59 [2·58-4·85]; OR 4·31 [3·02 - 6·14]).Low SES was associated with continuing or initiating physical inactivity and continuing smoking after NCD diagnosis. Reducing socioeconomic inequality in health behaviour changes should be prioritised and integrated into NCD-prevention programmes.Zhejiang University and Fundamental Research Funds for the Central Universities.
Blastocystis subtype 4 linked to gut microbiota stability
Authors: Folahan Feranmi
Journal: The Lancet Microbe (2022)

The gastrointestinal tract harbours many microbes, accounting for the highest population of microbiota in humans. It is believed that the presence of parasites in the gut is associated with infection and ultimately eliciting gastrointestinal-related symptoms such as inflammation, diarrhoea, and irritable bowel syndrome. However, an experimental colonisation study in mice has shown that a ubiquitous unicellular parasite—specifically a subtype of the genus Blastocystis—could be associated with benefits for gut health rather than being harmful.
Mapping emergency department asthma visits to identify poor-quality housing in New Haven, CT, USA: a retrospective cohort study
Authors: Elizabeth A Samuels, Richard Andrew Taylor, Akshay Pendyal, Abbas Shojaee, Anne S Mainardi, Evan R Lemire, Arjun K Venkatesh, Steven L Bernstein, Adam L Haber
Journal: The Lancet Public Health (2022)
Predictors and associations of the persistent airflow limitation phenotype in asthma: a post-hoc analysis of the ATLANTIS study
Authors: Tessa M Kole, Elise Vanden Berghe, Monica Kraft, Judith M Vonk, Martijn C Nawijn, Salman Siddiqui, Kai Sun, Leonardo M Fabbri, Klaus F Rabe, Kian Fan Chung, Gabriele Nicolini, Alberto Papi, Chris Brightling, Dave Singh, Thys van der Molen, Sven-Erik Dahlén, Alvar Agusti, Rosa Faner, Jadwiga A Wedzicha, Gavin C Donaldson, Ian M Adcock, Lies Lahousse, Huib A M Kerstjens, Maarten van den Berge, P. Badorrek, M. Broeders, W.G. Boersma, A. Chetta, A. Cukier, M. D'Amato, R. Djukanovic, M.P. Foschino, C. Gessner, N. Hanania, R. Martin, S. Milleri, R. Olivenstein, P. Paggiaro, E. Pizzichini, V. Plaza Moral, D.S. Postma, N. Scichilone, R. Schilz, A. Spanevello, R. Stelmach, J.S. Vroegop, O.S. Usmani, Q. Zhang, H. Ahmed, D. Allen, S. Ballereau, M.K. Batuwitage, A. Bedding, A.F. Behndig, A. Berglind, A. Berton, J. Bigler, M.J. Boedigheimer, K. Bønnelykke, P. Brinkman, A. Bush, D. Campagna, C. Casaulta, A. Chaiboonchoe, T. Davison, B. De Meulder, I. Delin, P. Dennison, P. Dodson, L. El Hadjam, D. Erzen, C. Faulenbach, K. Fichtner, N. Fitch, E. Formaggio, M. Gahlemann, G. Galffy, D. Garissi, T. Garret, E. Guillmant-Farry, E. Henriksson, U. Hoda, J.M. Hohlfeld, X. Hu, A. James, K. Johnson, N. Jullian, G. Kerry, M. Klüglich, R. Knowles, J.R. Konradsen, K. Kretsos, L. Krueger, A-S. Lantz, C. Larminie, P. Latzin, D. Lefaudeux, N. Lemonnier, L.A. Lowe, R. Lutter, A. Manta, A. Mazein, L. McEvoy, A. Menzies-Gow, N. Mores, C.S. Murray, K. Nething, U. Nihlén, R. Niven, B. Nordlund, S. Nsubuga, J. Pellet, C. Pison, G. Praticò, M. Puig Valls, K. Riemann, J.P. Rocha, C. Rossios, G. Santini, M. Sagi, S. Scott, N. Sehgal, A. Selby, P. Söderman, A. Sogbesan, F. Spycher, S. Stephan, J. Stokholm, M. Sunther, M. Szentkereszty, L. Tamasi, K. Tariq, S Valente, W.M. Van Aalderen, C.M. Van Drunen, J. Van Eyll, A. Vyas, W. Yu, W. Zetterguist, Z. Zolkipli, A.H. Zwinderman, A. Agusti, J.A. Wedzicha, G.C. Donaldson, R. Faner, R. Breyer-Kohansal, A.H. Maitland-van der Zee, E. Melén, J.P. Allinson, L.E.G.W. Vanfleteren, J. Vestbo, I.M. Adcock, L. Lahousse, M. Van den Berge, P. Alter, F. Barbe, C.E. Brightling, M.K. Breyer, O.C. Burghuber, M. Casas, K.F. Chung, B.G. Cosío, F. Crispi, J. De Batlle, J.W. Fitting, J. Garcia, J. Hallberg, S. Hartl, D. Jarvis, A. Mathioudakis, L. Nicod, A. Papi, A. Ritchie, T. Sigsgaard, P.J. Sterk, A. Ullman, K. Vellvé, C. Vogelmeier, A.M. Wheelock, C.E. Wheelock, A. Spanevello
Journal: The Lancet Respiratory Medicine (2022)
Haploidentical bone marrow transplantation in patients with relapsed or refractory severe aplastic anaemia in the USA (BMT CTN 1502): a multicentre, single-arm, phase 2 trial
Authors: Amy E DeZern, Mary Eapen, Juan Wu, Julie-An Talano, Melhem Solh, Blachy J Dávila Saldaña, Chatchada Karanes, Mitchell E Horwitz, Kanwaldeep Mallhi, Sally Arai, Nosha Farhadfar, Elizabeth Hexner, Peter Westervelt, Joseph H Antin, H Joachim Deeg, Eric Leifer, Robert A Brodsky, Brent R Logan, Mary M Horowitz, Richard J Jones, Michael A Pulsipher
Journal: The Lancet Haematology (2022)
Prevalence of suicidal ideation and self-harm behaviours in children aged 12 years and younger: a systematic review and meta-analysis
Authors: Marie-Claude Geoffroy, Samantha Bouchard, Megan Per, Bassam Khoury, Elise Chartrand, Johanne Renaud, Gustavo Turecki, Ian Colman, Massimiliano Orri
Journal: The Lancet Psychiatry (2022)